ID:REN3A_HUMAN DESCRIPTION: RecName: Full=Regulator of nonsense transcripts 3A; AltName: Full=Nonsense mRNA reducing factor 3A; AltName: Full=Up-frameshift suppressor 3 homolog A; Short=hUpf3; FUNCTION: Involved in nonsense-mediated decay (NMD) of mRNAs containing premature stop codons by associating with the nuclear exon junction complex (EJC) and serving as link between the EJC core and NMD machinery. Recruits UPF2 at the cytoplasmic side of the nuclear envelope and the subsequent formation of an UPF1-UPF2- UPF3 surveillance complex (including UPF1 bound to release factors at the stalled ribosome) is believed to activate NMD. However, UPF3A is shown to be only marginally active in NMD as compared to UPF3B. Binds spliced mRNA upstream of exon-exon junctions. In vitro, weakly stimulates translation. SUBUNIT: Found in a post-splicing messenger ribonucleoprotein (mRNP) complex. Associates with the exon junction complex (EJC). Interacts with UPF2 and RBM8A. INTERACTION: Q9Y5S9:RBM8A; NbExp=4; IntAct=EBI-521530, EBI-447231; Q92900:UPF1; NbExp=4; IntAct=EBI-521530, EBI-373471; SUBCELLULAR LOCATION: Nucleus. Cytoplasm. Note=Shuttling between the nucleus and the cytoplasm. TISSUE SPECIFICITY: Isoform 1 is strongly expressed in testis, uterus, muscle, fetal brain and spinal cord. Isoform 2 is strongly expressed in fetal brain and spinal cord. SIMILARITY: Belongs to the RENT3 family.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q9H1J1
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.